The proposed study is designed to obtain a basic understanding of drugs that may act on GABA receptors in the mammalian central nervous system. Due to the complex nature of the synaptic connections within the central nervous system, studies involving an intact system are nearly impossible to interpret in terms of drug-receptor mechanisms at the cellular level. This problem has been overcome by the characterization of a mammalian GABA-receptor isolated on the soma of cat primary afferent neurons (Gallagher, Higashi and Nishi, 1978). By coupling differential interference microscopy with the electrophysiological techniques already employed one can obtain a quantitative analysis of the cellular mechanism(s) by which drugs may alter the GABA-receptor interaction. Three groups of drugs will be used in this study: 1) anionic transport inhibitors; 2) anti-convulsants; and 3) psychoactive agents. These have been chosen to explore the possibility that an altered chloride permeability may be involved in those disease states which have been implicated with the gabergic system; these include: epilepsy, schizophrenia, Parkinson's disease and Huntington's disease.